Plastic changes in sensory inputs to rat substantia gelatinosa neurons following peripheral inflammation

Nakatsuka, Terumasa; Park, Jin-Soo; Kumamoto, Eiichi; Tamaki, Toru; Yoshimura, Michihiro

doi:10.1016/s0304-3959(99)00037-8

Cited by 79 publications

(89 citation statements)

References 43 publications

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“…5C). Recording of the synaptic transmission between the C-fiber terminal and the secondorder neuron was carried out in lamina II, a translucent easily identified band in the superficial dorsal horn of spinal cord (38). We measured the miniature excitatory postsynaptic currents (mEPSCs) in the presence of tetrodotoxin (0.5 μM) and found that SNC80 and DAMGO reduced the frequency but not the amplitude of mEPSCs (Fig.…”

Section: Resultsmentioning

confidence: 99%

Coexpression of δ- and μ-opioid receptors in nociceptive sensory neurons

Wang

Zhao²,

Zhong

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

192

204

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Morphine-induced analgesia and antinociceptive tolerance are known to be modulated by interaction between δ-opioid receptors (DORs) and μ-opioid receptors (MORs) in the pain pathway. However, evidence for expression of DORs in nociceptive small-diameter neurons in dorsal root ganglia (DRG) and for coexistence of DORs with MORs and neuropeptides has recently been challenged. We now report, using in situ hybridization, single-cell PCR, and immunostaining, that DORs are widely expressed not only in large DRG neurons but in small ones and coexist with MORs in peptidergic small DRG neurons, with protachykinin-dependent localization in large dense-core vesicles. Importantly, both DOR and MOR agonists reduce depolarization-induced Ca 2+ currents in single small DRG neurons and inhibit afferent C-fiber synaptic transmission in the dorsal spinal cord. Thus, coexistence of DORs and MORs in small DRG neurons is a basis for direct interaction of opioid receptors in modulation of nociceptive afferent transmission and opioid analgesia.

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Section: Resultsmentioning

confidence: 99%

Coexpression of δ- and μ-opioid receptors in nociceptive sensory neurons

Wang

Zhao²,

Zhong

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

192

204

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“…In the spinal cord, synaptic transmission and sensory circuitry is shown to be unstable, changing easily the efficacy of synaptic transmission and termination of the inputs following pathological conditions (see Okamoto, 2000;Nakatsuka, 1999;Ito, 2000). Profound flexibility in the sensory system might be due to the primitivity of the system.…”

Section: Discussionmentioning

confidence: 99%

“…We have investigated the synaptic plasticity observed in various pathological conditions such as sciatic nerve transection (Okamoto, 2000), inflammation (Nakatsuka, 1999) and ovariectomy (OVX) (Ito, 2000). In this section some data are demonstrated to briefly show how the sensory transmission was modified by OVX using slice preparations from OVX rats.…”

Section: Synaptic Responses In the Spinal Cord Under Pathological Conmentioning

confidence: 99%

“…Inflamed rats were made by injection of complete Freund's adjuvant (CFA) to the hind paw (Nakatsuka, 1999). The rats showed significant hyperalgesia when tested by the von Frey hair test and the effect lasted for at least 2 weeks.…”

Section: Sprouting Of Ab Afferent Following Inflammationmentioning

confidence: 99%

“…In addition, a variety of plastic changes in the spinal sensory pathway has been elucidated using chronic pain models, including inflammation, sciatic nerve transection and ovariecotomy. In chronic inflammation model rats, the large sensory afferent fiber, Ab sprouts into lamina II, substantia gelatinosa (SG) (Nakatsuka, 1999). Considering that the non-noxious information is carried to the deep dorsal horn neurons by Ab afferents and SG plays an important role in the processing of the nociceptive transmission, the sprouting of Ab afferent to SG might be an underlying mechanism for allodynia observed in inflamed patients.…”

Section: Introductionmentioning

confidence: 99%

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In vivo and in vitro Patch-clamp Recording Analysis of the Process of Sensory Transmission in the Spinal Cord and Sensory Cortex

Yoshimura

Doi

Mizuno

et al. 2005

J. Physiol. Anthropol.

Self Cite

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Following the integration and modification of the sensory inputs in the spinal cord, the information is transmitted to the primary sensory cortex where the integrated information is further processed and perceived. Processing of the sensory information in the spinal cord has been intensively investigated. However, the mechanisms of how the inputs are processed in the cortex are still unclear. To know the correlation of the sensory processing in the dorsal horn and cortex, in vivo and in vitro patch-clamp recordings were made from rat dorsal horn and sensory cortex. Although dorsal horn neurons showed spontaneous and evoked EPSCs by noxious and non-noxious stimuli, most somatosensory neurons located at 100 to 1000 mm from the surface of the cortex exhibited an oscillatory activity and received synaptic inputs from nonnoxious but not noxious receptors. These observations suggest that the synaptic responses in cortical neurons are processed in a more complex manner; and this may be due to the reciprocal synaptic connection between thalamus and cortex.

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N⁶‐Methyladenosine Demethylase FTO Contributes to Neuropathic Pain by Stabilizing G9a Expression in Primary Sensory Neurons

et al. 2020

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Nerve injury‐induced change in gene expression in primary sensory neurons of dorsal root ganglion (DRG) is critical for neuropathic pain genesis. N 6 ‐methyladenosine (m 6 A) modification of RNA represents an additional layer of gene regulation. Here, it is reported that peripheral nerve injury increases the expression of the m 6 A demethylase fat‐mass and obesity‐associated proteins (FTO) in the injured DRG via the activation of Runx1, a transcription factor that binds to the Fto gene promoter. Mimicking this increase erases m 6 A in euchromatic histone lysine methyltransferase 2 ( Ehmt2 ) mRNA (encoding the histone methyltransferase G9a) and elevates the level of G9a in DRG and leads to neuropathic pain symptoms. Conversely, blocking this increase reverses a loss of m 6 A sites in Ehmt2 mRNA and destabilizes the nerve injury‐induced G9a upregulation in the injured DRG and alleviates nerve injury‐associated pain hypersensitivities. FTO contributes to neuropathic pain likely through stabilizing nerve injury‐induced upregulation of G9a, a neuropathic pain initiator, in primary sensory neurons.

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Plastic changes in sensory inputs to rat substantia gelatinosa neurons following peripheral inflammation

Cited by 79 publications

References 43 publications

Coexpression of δ- and μ-opioid receptors in nociceptive sensory neurons

Coexpression of δ- and μ-opioid receptors in nociceptive sensory neurons

In vivo and in vitro Patch-clamp Recording Analysis of the Process of Sensory Transmission in the Spinal Cord and Sensory Cortex

N⁶‐Methyladenosine Demethylase FTO Contributes to Neuropathic Pain by Stabilizing G9a Expression in Primary Sensory Neurons

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Plastic changes in sensory inputs to rat substantia gelatinosa neurons following peripheral inflammation

Cited by 79 publications

References 43 publications

Coexpression of δ- and μ-opioid receptors in nociceptive sensory neurons

Coexpression of δ- and μ-opioid receptors in nociceptive sensory neurons

In vivo and in vitro Patch-clamp Recording Analysis of the Process of Sensory Transmission in the Spinal Cord and Sensory Cortex

N6‐Methyladenosine Demethylase FTO Contributes to Neuropathic Pain by Stabilizing G9a Expression in Primary Sensory Neurons

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N⁶‐Methyladenosine Demethylase FTO Contributes to Neuropathic Pain by Stabilizing G9a Expression in Primary Sensory Neurons